The efficacy of conduction system pacing and conventional strategies under bundle branch block depends on the resynchronisation metric: a computational study
M Kariman, C Augustin, G PlankAbstract
Introduction
Interventricular dyssynchrony is a hallmark of heart failure and a contributor to reduced cardiac output. Cardiac resynchronisation therapy (CRT) with biventricular pacing (BiVP) enhances electrical synchrony but remains limited by variable response rates. Conduction system pacing (CSP), as an alternative to BiVP, offers more physiological ventricular activation and improved synchrony in patients with suboptimal response to CRT. However, assessing the degree of resynchronisation of these strategies using conventional clinical indices remains ambiguous. For a more accurate assessment of resynchronization efficacy, we used high-fidelity computational simulations to compare various CSP modalities and established strategies, employing a combination of conventional clinical and novel computational metrics to gain mechanistic insight into these differences.
Method
Using a four-chamber model of human electrophysiology, we systematically evaluated the resynchronisation efficacy of different CSP modalities comprising left and right bundle branch pacing (LBBP and RBBP), alongside conventional strategies such as BiVP, under bundle branch block conditions. Pacing efficacy of each modality was assessed using three complementary metrics capturing distinct electrophysiological perspectives: (1) clinical ECG markers, including QRS duration, His–ventricular (H–V) interval, interpeak interval between leads V6 and V1 (V6V1II), and V6 R-wave peak time (V6RWPT); (2) high density activation maps; and (3) a novel mechanistic metric, ventricular activation velocity, to characterize synchrony over time during ventricular depolarization.
Results
Our simulations revealed that the apparent efficacy of pacing strategies was dependent on the assessment metric. For example, under focal left bundle branch block conditions, BiVP produced improvements in ECG-based markers, such as narrowing QRS duration from 120 to 90 ms and reducing V6RWPT from 53 to 10 ms, and matching activation velocity profiles, but produced activation maps that deviated strikingly from those during normal sinus activation. In contrast, LBBP also yielded improved ECG markers with activation patterns closely resembling normal sinus activation, but differences between left and right activation velocity profiles revealed a residual temporal mismatch between the ventricles, with activation velocity in the LV remaining reduced, highlighting that persistent dyssynchrony may not be fully captured by standard ECG markers alone.
Conclusion
Our findings indicate that the apparent efficacy of pacing strategies depends on the chosen assessment metric. While conventional ECG markers offer a rapid estimation of resynchronisation, they provide an incomplete view on the underlying electrical synchrony. Integrating conventional clinical makers with computational markers derived from patient-specific models may enable a more comprehensive and physiologically relevant evaluation of resynchronisation efficacy.